Tyrosinase deficiency prevents iris disease in B6. Tyrp1b GpnmbR150X mice. Intercrosses generated mice homozygous for various genotypic combinations of the Tyrp1b and GpnmbR150X mutations with the albino-inducing Tyrc-2J mutation. These mice were aged and analyzed by slit-lamp examination; representative B6.Tyrp1b GpnmbR150X eyes are shown. (A) The normally brown pigmented coat of a mouse on the left compared with a triple homozygous Tyrc-2J Tyrp1b GpnmbR150X mouse on the right. (B, D, F) Different views emphasize the clinical morphology of the albino iris. Eyes of B6 mice that are homozygous for the Tyrc-2J mutation only appear pink as they lack melanin, but otherwise the iris and its vasculature have normal morphology. (C, E, G) Homozygosity for Tyrc-2J completely prevents iris disease in B6.Tyrp1b GpnmbR150X Tyrc-2J mice. The iris morphology of the triple mutant is indistinguishable from that of B6 mice homozygous for Tyrc-2J only (compare 3B to 3C), lacks peripupillary abnormalities (compare 3D to 3E), and has a healthy uninterrupted vasculature (3F to 3G). n = 14 eyes, all 12+ months.
Anderson et al. BMC Biology 2006 4:20 doi:10.1186/1741-7007-4-20